History and exam

Key diagnostic factors

common

presence of risk factors

Key risk factors include a family history of asthma and a family history of atopic diseases, exposure to allergens (e.g., dust mites, pets), exposure to irritants (e.g., tobacco smoke), or personal history of atopic diseases (e.g., eczema, allergic rhinitis).[1]

expiratory wheezes

Audible on auscultation.[1] Precipitated by allergen exposure, infection (particularly viral), exposure to cold air, tobacco smoke, or particulates; worse with reactions such as hard laughter.[1]​ Emotions such as stress/anxiety may be associated with exacerbation of asthma symptoms, although these are more often a cause of breathing pattern disorder (dysfunctional breathing) in people with asthma.

Polyphonic, high-pitched expiratory wheezes are typical of asthma.

Distinguish wheezing from other respiratory noises, e.g., stridor or rattly breathing.[55] With more severe asthma, the wheezes may be audible without the use of a stethoscope. The absence of wheeze does not exclude asthma.[55]


Expiratory wheeze
Expiratory wheeze

Auscultation sounds: Expiratory wheeze



Polyphonic wheeze
Polyphonic wheeze

Auscultation sounds: Polyphonic wheeze


dyspnoea

Precipitated by allergen exposure, infection (particularly viral), exposure to cold air, tobacco smoke, or particulates; worse with reactions such as hard laughter.[1]​ Emotions such as stress/anxiety may be associated with exacerbation of asthma symptoms, although these are more often a cause of breathing pattern disorder (dysfunctional breathing) in people with asthma.

May wake patient from sleep.

cough

Precipitated by allergen exposure, infection (particularly viral), exposure to cold air, tobacco smoke, or particulates; worse with reactions such as hard laughter.[1]​ Emotions such as stress/anxiety may be associated with exacerbation of asthma symptoms, although these are more often a cause of breathing pattern disorder (dysfunctional breathing) in people with asthma.

May wake patient from sleep.

chest tightness

Precipitated by allergen exposure, infection (particularly viral), exposure to cold air, tobacco smoke, or particulates; worse with reactions such as hard laughter.[1]​ Emotions such as stress/anxiety may be associated with exacerbation of asthma symptoms, although these are more often a cause of breathing pattern disorder (dysfunctional breathing) in people with asthma.

May wake patient from sleep.

diurnal variability of symptoms

Symptoms that are worse at night or in the early morning; characteristic of the rhythmic nature of asthma.[1][79]

episodic symptoms

A number of studies highlight the diagnostic significance of episodic symptoms as an important predictor of asthma.[55][58]

historical record of variable peak expiratory flow (PEF) or FEV₁

A historical record of significantly lower FEV₁ or PEF during symptomatic episodes compared with asymptomatic periods provides objective confirmation of the obstructive nature of the episodic symptoms.[55]

nasal polyposis

Appear as single or multiple polyps in the nasal cavity.

recent upper respiratory tract infection

With a recent sinusitis or common cold, symptoms are typically exacerbated.

Risk factors

strong

family history

A parental history of asthma is a major risk factor for early development of asthma.[1][2]​​

Multiple genes are implicated that predispose people to hyper-responsiveness to environmental triggers.

allergens/irritants

Common allergens include cats, dogs, cockroaches, dust mites, fungal spores, and pollen from trees, weeds, and grass. Irritants include tobacco smoke and fumes from chemicals (e.g., bleach).[33]

Other indoor air pollutants linked to increased asthma symptoms and exacerbations include those from wood burning, natural gas, cooking, and evaporative volatile organic compounds.[24][25][26]

Workers commonly affected by occupational allergens and irritants include bakers, farmers, carpenters, and people involved in manufacturing plastics, foams, and glues.[34]​ See Occupational asthma.

atopic disease history

History of eczema, atopic dermatitis, and/or allergic rhinitis is strongly associated.[1][20] The progression from eczema/atopic dermatitis to allergic rhinitis to subsequent asthma has been termed the 'allergic or atopic march'.[35] Association is possibly due to genetic variants in shared susceptibility genes.[20][35]

cigarette smoking

Smoking increases the risk of developing asthma and is associated with a worse prognosis.[1][19][33][36]​ Patients with asthma who smoke have been found to have elevated levels and activation of neutrophils compared with non-smoking patients with asthma.[19]

vaping

Vaping (electronic nicotine delivery system or e-cigarette use) has been associated with higher rates of asthma and asthma exacerbations, and even reports of status asthmaticus.[21][37]​​[38]

It is thought to exert its effects by increasing the risk of obstructive lung function impairment.[21][22][23]​​

respiratory viral infection early in life

Infection with human respiratory syncytial virus or human rhinovirus in early life increases the likelihood of developing asthma in those at risk.[18]

Moreover, viral infection may be detected in up to 58% of patients with an asthma exacerbation.[39]

nasal polyposis

The prevalence of chronic rhinosinusitis with nasal polyps is higher in patients with asthma compared with the general population, and is associated with greater disease severity.[40][41] The two conditions share pathophysiological processes including airway remodelling and eosinophilia.[41] Chronic rhinosinusitis with nasal polyps is more commonly associated with adult early- or late-onset versus childhood asthma.[40]

low socioeconomic status

Socioeconomically disadvantaged groups are more likely to live in areas with the poorest air quality and worst housing conditions, while being exposed to more psychosocial stress and having poorer diets.[10]​ Socioeconomic status (e.g., education and income) can also affect access to healthcare. These factors increase the risk of asthma, poor asthma control, and acute exacerbations.

weak

obesity

High body mass index increases the likelihood of developing asthma, while significant weight loss can improve asthma control.[42][43]​ One study found that adults with a history of, or current, asthma were significantly less likely to be physically active than those without asthma.[44][45]

Postulated mechanisms include reduced lung and tidal volume (promoting airway narrowing), low-grade systemic inflammation, effect of comorbidities, or a common aetiology.[46][47]

Growing evidence suggests a specific, female-predominant phenotype of asthma in people with obesity, whereby patients are less responsive to typical asthma medications and generally have a poorer prognosis.[42][43][48]

gastro-oesophageal reflux

Prevalent in patients with poorly controlled asthma.[49] The link between gastro-oesophageal reflux disease (GORD) and the development of asthma remains unclear, but could be related to chronic irritation and inflammation of the airways following exposure to gastric contents.[50][51] One Cochrane review found that treatment for GORD moderately improved lung function and use of rescue medication in patients with moderate-to-severe asthma and comorbid GORD; however, the effect of GORD treatment on exacerbations and hospital utilisation is uncertain.[52]

obstructive sleep apnoea

The prevalence of obstructive sleep apnoea (OSA) in patients with asthma is approximately two to three times higher than in the general population.[53] Both conditions share risk factors including obesity, rhinitis, and gastro-oesophageal reflux disease.[51][53] Patients with asthma should be screened for symptoms suggestive of OSA and, if positive, referred for sleep testing to confirm the diagnosis.[54]

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